@unpublished{20465,
  abstract     = {For tissues to spread, they must be deformable while maintaining their structural integrity. How these opposing requirements are balanced within spreading tissues is not yet well understood. Here, we show that keratin intermediate filaments function in epithelial spreading by adapting tissue mechanical resilience to the stresses arising in the tissue during the spreading process. By analysing the expansion of the enveloping cell layer (EVL) over the large yolk cell in early zebrafish embryos in vivo, we found that keratin network maturation in EVL cells is promoted by stresses building up within the spreading tissue. Through genetic interference and tissue rheology experiments, complemented by a vertex model with mechanochemical feedback, we demonstrate that stress-induced keratin network maturation in the EVL increases tissue viscosity, which is essential for preventing tissue rupture. Interestingly, keratins are also required in the yolk cell for mechanosensitive actomyosin network contraction and flow, the force-generating processes pulling the EVL. These dual mechanosensitive functions of keratins enable a balance between pulling force production in the yolk cell and the mechanical resilience of the EVL against stresses generated by these pulling forces, thereby ensuring uniform and robust tissue spreading.},
  author       = {Naik, Suyash and Keta, Yann-Edwin and Pranjic-Ferscha, Kornelija and Hannezo, Edouard B and Henkes, Silke and Heisenberg, Carl-Philipp J},
  booktitle    = {bioRxiv},
  title        = {{Keratins coordinate tissue spreading by balancing spreading forces with tissue material properties}},
  doi          = {10.1101/2025.02.14.638262},
  year         = {2025},
}

@article{15048,
  abstract     = {Embryogenesis results from the coordinated activities of different signaling pathways controlling cell fate specification and morphogenesis. In vertebrate gastrulation, both Nodal and BMP signaling play key roles in germ layer specification and morphogenesis, yet their interplay to coordinate embryo patterning with morphogenesis is still insufficiently understood. Here, we took a reductionist approach using zebrafish embryonic explants to study the coordination of Nodal and BMP signaling for embryo patterning and morphogenesis. We show that Nodal signaling triggers explant elongation by inducing mesendodermal progenitors but also suppressing BMP signaling activity at the site of mesendoderm induction. Consistent with this, ectopic BMP signaling in the mesendoderm blocks cell alignment and oriented mesendoderm intercalations, key processes during explant elongation. Translating these ex vivo observations to the intact embryo showed that, similar to explants, Nodal signaling suppresses the effect of BMP signaling on cell intercalations in the dorsal domain, thus allowing robust embryonic axis elongation. These findings suggest a dual function of Nodal signaling in embryonic axis elongation by both inducing mesendoderm and suppressing BMP effects in the dorsal portion of the mesendoderm.},
  author       = {Schauer, Alexandra and Pranjic-Ferscha, Kornelija and Hauschild, Robert and Heisenberg, Carl-Philipp J},
  issn         = {1477-9129},
  journal      = {Development},
  number       = {4},
  pages        = {1--18},
  publisher    = {The Company of Biologists},
  title        = {{Robust axis elongation by Nodal-dependent restriction of BMP signaling}},
  doi          = {10.1242/dev.202316},
  volume       = {151},
  year         = {2024},
}

@article{7001,
  author       = {Schwayer, Cornelia and Shamipour, Shayan and Pranjic-Ferscha, Kornelija and Schauer, Alexandra and Balda, M and Tada, M and Matter, K and Heisenberg, Carl-Philipp J},
  issn         = {1097-4172},
  journal      = {Cell},
  number       = {4},
  pages        = {937--952.e18},
  publisher    = {Cell Press},
  title        = {{Mechanosensation of tight junctions depends on ZO-1 phase separation and flow}},
  doi          = {10.1016/j.cell.2019.10.006},
  volume       = {179},
  year         = {2019},
}

@article{1912,
  abstract     = {Kupffer's vesicle (KV) is the zebrafish organ of laterality, patterning the embryo along its left-right (LR) axis. Regional differences in cell shape within the lumen-lining KV epithelium are essential for its LR patterning function. However, the processes by which KV cells acquire their characteristic shapes are largely unknown. Here, we show that the notochord induces regional differences in cell shape within KV by triggering extracellular matrix (ECM) accumulation adjacent to anterior-dorsal (AD) regions of KV. This localized ECM deposition restricts apical expansion of lumen-lining epithelial cells in AD regions of KV during lumen growth. Our study provides mechanistic insight into the processes by which KV translates global embryonic patterning into regional cell shape differences required for its LR symmetry-breaking function.},
  author       = {Compagnon, Julien and Barone, Vanessa and Rajshekar, Srivarsha and Kottmeier, Rita and Pranjic-Ferscha, Kornelija and Behrndt, Martin and Heisenberg, Carl-Philipp J},
  journal      = {Developmental Cell},
  number       = {6},
  pages        = {774 -- 783},
  publisher    = {Cell Press},
  title        = {{The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ}},
  doi          = {10.1016/j.devcel.2014.11.003},
  volume       = {31},
  year         = {2014},
}